Hepatitis B Virus and DNA Repair We and others have previously reported that p53 can modulate nucleotide excision repair. Using a host reactivation assay, our preliminary data indicate that HBx inhibits reactivation, i.e., repair of the ultraviolet light (UV-C, 254 nm) damage plasmid. This leads to the hypothesis that HBx inhibits p53 binding to XPB or XPD DNA helicases in the basal transcription-nucleotide excision repair complex, TFIIH. We have previously demonstrated that HBx protein inhibits in vitro p53 binding to XPB. HBx binds to XPB. HBx binds to the carboxyl terminus of p53 which also is the site of XPB binding. We are currently investigating the hypothesis that HBx binds to other members of the TFIIH multiprotein complex. We are attempting to obtain crystals of HBVX and co-crystals of its binding partners for fine detail structural analysis.